This study focuses on the transcriptional regulation of HIV-1 replication in alveolar macrophages. Alveolar macrophages from uninflamed lung inhibit HIV-1 replication by expressing a 16kDa inhibitory form of transcription factor C/EBPB (also called NF-IL6 and LIP) producing latent HIV-I infection in the lung. The inflammatory response to tuberculosis reduces C/EBPB expression, derepressing the HIV-1 long terminal repeat and induces another member of the C/EBP transcription factor family which supports high level HIV-1 replication in the lung. The lab was used for the following: DNA isolation, DNA sequencing (automated), ELISA, oligonucleotide synthsis, PCR, recombinant DNA techniques, RNA isolation, Southern analysis, Western analysis, bronchoalveolar lavage processing, and use of laminar flow hoods.